Background/Objectives: Multiple system atrophy (MSA) presents a challenging diagnosis due to its clinical overlap with other neurodegenerative disorders, especially other α-synucleinopathies. The main purpose of this systematic review and meta-analysis was to assess neurofilament light chain (NfL) differences in the CSF and blood of patients with MSA versus the healthy control group (HC), patients with Parkinson’s disease (PD) and patients with Lewy body dementia (LBD). Secondarily, the diagnostic metrics of CSF and circulating NfL in MSA versus HC, PD, LBD, progressive supranuclear palsy (PSP) and corticobasal degeneration (CBD) were discussed. Methods: MEDLINE and EMBASE were thoroughly searched for relevant case-control studies. Standardized mean differences (SMDs) were calculated separately for CSF and blood NfL per comparison. Statistical heterogeneity was assessed based on the Q and I^2 statistics. Results: Twenty-five relevant studies were retrieved. Quantitative syntheses revealed elevated CSF and circulating NfL levels in individuals with MSA versus HC [SMD = 1.80 (95%CI = 1.66, 1.94) and SMD = 2.00 (95%CI = 1.36, 2.63), respectively] versus PD [SMD = 1.65 (95%CI = 1.26, 2.03) and SMD = 1.63 (95%CI = 0.84, 2.43), respectively] as well as versus LBD [SMD = 1.17, (95%CI = 0.71, 1.63) and SMD = 0.65 (95%CI = 0.30, 1.00), respectively]. Diagnostic accuracy was outstanding for CSF and blood NfL in MSA versus HC and PD, and it was moderate in MSA versus LBD. On the other hand, it was suboptimal in MSA vs. PSP and CBD. Conclusions: Both CSF and circulating NfL levels are elevated in MSA compared to HC, PD and LBD. To achieve optimal diagnostic properties, further work is required in the standardization of processes and the establishment of reference NfL intervals and/or thresholds.

Due to the occlusion of the anterior choroidal artery (AChA), ischemic strokes are described with the classic clinical triad, namely hemiplegia, hemianesthesia, and homonymous hemianopsia. The aim of this study is to document the characteristic clinical presentation and course of AChA infract cases. We describe five cases with acute infarction in the distribution of the AChA, admitted to the Neurological Department of the University General Hospital of Larissa. Results: All cases presented with hemiparesis and lower facial nerve palsy, while four of them had dysarthria, and two patients exhibited ataxia. Two cases underwent intravenous thrombolysis. A notable feature was the worsening of the clinical course, specifically the exacerbation of upper limb weakness within 48 h. Stabilization occurred after the third day, with the final development of a more severe clinical presentation than the initial one. Additionally, muscle weakness was more severe in the upper limb than in the lower limb. The recovery of upper limb function was poor in the three-month follow-up for the four cases. While vascular brain episodes are characterized by sudden onset, in AChA infraction, the clinical onset can be gradually developed over a few days, with a greater burden on the upper limb and poorer recovery.

Background/Objectives: Mild cognitive impairment in Parkinson’s disease (PD-MCI) affects approximately 20–50% of patients, and it is associated with an increased risk of dementia. Computer-assisted cognitive interventions (CCTs) have been proposed as a promising method of improving cognitive function in these patients. This review aims to (1) demonstrate the effectiveness of computer-based intervention in PD-MCI, and (2) determine the most effective iteration. Methods: A review was performed using PubMed, Google Scholar, and ScienceDirect. Full texts of randomized clinical trials (RCTs) involving CCT intervention in PD-MCI and published in English language journals between 2014 and 2024 were included. Results: Of the 747 studies identified, 6 studies fulfilled the eligibility criterion for this review. Patients receiving CCTs showed significant improvements in global cognition and executive function, while mood was not significantly affected in most studies. Conclusions: CCT improves cognitive functions, particularly memory and executive abilities, but has little effect on mood. Although the results are encouraging, there are potential methodological biases that need to be considered.

We investigated associations between apolipoprotein E (APOE) alleles and motor manifestations in Alzheimer’s dementia (AD) capitalizing on National Alzheimer’s Coordinating Center data: the baseline evaluations of older adults (≥60 years) with a diagnosis of AD were analyzed. Those with a concomitant diagnosis Parkinson’s disease or other parkinsonian syndrome, and those treated with anti-parkinsonian agents were excluded. Three APOE groups were formed: APOE2 (APOE2 carriers), APOE3 (APOE3/APOE3) and APOE4 (APOE4/APOE4, APOE4/APOE3). UPDRS-III was used to assess the presence or absence of motor signs in 9 domains. Adjusted binary logistic models featuring the three APOE groups as exposures and motor domains as outcomes were estimated. There were 389 individuals in the APOE2, 1799 in the APOE3 and 2791 in the APOE4 groups. Compared to the APOE2 group, individuals in the APOE4 group had lower odds of having at least one motor sign [0.64 (0.50–0.82)]. Among motor signs, rigidity [0.53 (0.34–0.81)], bradykinesia [0.56 (0.40–0.77)], impaired chair rise [0.54 (0.37–0.78)] and impaired posture-gait [0.54 (0.36, 0.81)] exhibited significant associations. Exploratory analyses featuring APOE genotypes suggested dose–response relationships for both APOE2 and APOE4. In conclusion, APOE2 confers a risk towards motor (mainly parkinsonian) signs in AD. APOE4 may have a protective effect.

Purpose: Motor signs are frequently observed over the clinical course of Alzheimer’s disease (AD). We explored the potential clinical associations of motor manifestations in AD. Methods: Our sample consisted of older adults (≥ 60 years) with AD from NACC. Individuals with Parkinson’s disease or other Parkinsonian syndrome or under anti-parkinsonian agents were excluded. UPDRS III was used to assess motor signs in nine domains: hypophonia; masked facies; resting tremor; action/postural tremor; rigidity; bradykinesia; impaired chair rise; impaired posture/gait; postural instability. A global motor variable assessed the presence of at least one motor sign. Binary logistic models were estimated for the global (primary) and individual motor domain variables (secondary outcomes). Results: A total of 4771 older, predominantly female, well-educated participants were analysed: 3556 without (75.4 ± 7.6 years, 45.6% males) and 1215 with motor manifestations (79.4 ± 7.8 years, 44.4% males). The most influential risk factor for motor manifestations in AD was the Clinical Dementia Rating stage: stage one increased the odds of motor signs by ~ 44%, stage two by ~ 168% and stage three by ~ 437%. Each additional point on the Geriatric Depression Scale elevated the odds of motor manifestations by ~ 5%, whereas each additional point on the Mini-Mental State Examination decreased these odds by ~ 2.5%. Cerebrovascular disease (by ~ 44%), diabetes mellitus (by ~ 25%), traumatic brain injury (by ~ 30%), alcohol abuse (by ~ 33%), anxiolytics (by ~ 36%), antidepressants (by ~ 31%), antipsychotics (by ~ 48%) and β-blockers (by ~ 33%) elevated the odds of motor manifestations. Angiotensin II receptor blockers decreased the odds of motor manifestations (by ~ 33%). Conclusion: Disease progression constitutes the most crucial clinical risk factor for motor manifestations in AD.

Background and Objectives: The interplay between motor tasks and cognition in Alzheimer’s dementia (AD) remains insufficiently characterised. We hypothesised that prefrontal-mediated cognitive functions could contribute to motor impairments in older adults with AD. Materials and Methods: Cross-sectional data from the National Alzheimer’s Coordinating Centre (NACC) were analysed. Our sample included older adults (≥60 years) with a baseline diagnosis of AD. The Unified Parkinson’s Disease Rating Scale Part-III was used to assess the presence or absence of motor signs. Episodic memory, language, confrontation naming, attention, processing speed, and executive function were assessed using a neuropsychological battery. Binary logistic models examined the relationship between cognitive performance and motor manifestations. Results: Of 44,713 NACC participants, 5124 individuals with complete covariate data were included in the analysis, 1339 with and 3785 without motor signs. Participants were predominantly female (~55%), with an average age of 76.5 ± 7.9 years and mean education of 14.2 ± 3.7 years. The presence of motor manifestations was related to slower processing speed (Trail Making Test—Part A) and impaired executive function (Trail Making Test—Part B). No covariate modified these associations. Among specific motor domains, impaired chair rise was related to executive dysfunction, whereas postural instability, impaired posture–gait, and bradykinesia were related to slower mental processing. Hypophonia, masked facies, resting tremor, action–postural tremor and rigidity were not associated with any cognitive measure. Conclusions: Processing speed and, to a lesser extent, executive function emerged as the main cognitive functions associated with motor manifestations in older adults with AD. Further research is needed to clarify the nature of this association, including potential causal pathways.